FOXA1 mediates p Activation during Cellular Senescence

As you can see below, all referees appreciate the demonstration that FoxA1 promotes cellular senescence via the transcriptional activation of p16INK4a. However, the principal concern expressed by at least two reviewers is that the study remains too preliminary at this stage. In particular, the molecular mechanism by which FoxA1 modulates PRC function remains vague and requires further substantiation. Furthermore, the interesting aspect that the core region of the predicted FoxA1 binding motif at the distal interaction site in the p16 promoter carries a Diabetesassociated SNP is not sufficiently developed. Although we appreciate that a thorough analysis might be beyond the scope of the current manuscript, we nevertheless would like to stress that this potential link to Diabetes does add significantly to the general interest of the study. The issues mentioned above would have to be addressed by a considerable amount of additional work. However, since this appears feasible based on the constructive suggestions made by the referees, we would be willing to grant the opportunity to significantly extend and revise the current manuscript. As this will entail time-consuming experimentation, we would understand if you might decide to seek potential rapid publication elsewhere.